The overexpression of ab modulates the expression of a significant proportion of the genome to block differentiation, repress ecdysone signalling (potentially through direct association with the ecdysone receptor coactivator Tai), and promote cell survival and proliferation; whilst loss of scrib induces aPKC-dependent Yki activity to promote tumour overgrowth, and JNK signalling to promote invasion. Here, SCRIB is linked to neoplasm.